nsulin. In addition, individuals with Werner Syndrome develop progressive thickening and loss of elasticity of artery walls. Some affected individuals may also be susceptible to developing certain tumors. Progressive arteriosclerosis, malignancies, and associated abnormalities may result in potentially life-threatening complications by approximately the fourth or firth decade of life due to Werner syndrome.
             Just recently, an international team of geneticists, led by Gerard Schellenberg of the Veterans Affairs Puget Sound Health Care System in Seattle, discovered the gene at fault in Werner syndrome. Aging experts are already delighted by this magnificent finding. This is important because it is the first time that any gene that has been associated with aging has been identified. One reason for the excitement is that the structure of the protein encoded by the gene indicates that it is a helicase, an enzyme that acts to unwind DNA and sometimes RNA in order to facilitate such processes as the replication, repair, transcription, and recombination of DNA. Some helicases may also be important in ensuring the accuracy of chromosomal segregation. Precisely which subset of these functions is critical in producing the pathology of Werner syndrome is not yet known. This suggests that the mutations that cause Werner Syndrome may exert their harmful effects by upsetting one or another of those activities. The fact that these helicase mutations are responsible for the disorder, leads support to several lines of evidence that indicate that the somatic cells of Werner Syndrome patients are especially prone to mutations. By testing out what does happen, researchers hope they will eventually be able to design a treatment that slows the aging process and cures Werner syndrome.
             The gene may also yield insights into cancer, because Werner syndrome patients suffer from many forms of cancer or rare tumors. From this, it can be concluded t...